Department of Clinical Laboratory, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Department of Clinical Laboratory, Suzhou Wuzhong People's Hospital, Suzhou, China.
Platelets. 2022 Oct 3;33(7):998-1008. doi: 10.1080/09537104.2022.2026907. Epub 2022 Jan 24.
Thrombocytopenia or platelet dysfunction is a risk factor for severe infection. () releases a variety of virulence factors especially toxic shock syndrome toxin 1 (TSST-1), which may cause toxic shock syndrome. , when carrying the gene, is more prone to cause toxic shock syndrome and is responsible for an especially high rate of mortality. However, the effect of TSST-1 protein on platelets is unknown. Patients with the gene positive bacteremia showed more serious infection, higher mortality and lower platelet count. The gene positive strains induce more platelet apoptosis and activation and corresponding up-regulation of Bak and down-regulation of Bcl-XL in addition to the activation of Caspase-3. C57BL/6 mice infected with the gene positive strains resulted in both a decrease in platelet count and an increase in platelet apoptosis and/or activation events and mortality. Moreover, TSST-1 protein, encoded by gene, caused the decrease of platelet count, the increase of platelet apoptosis and activation events and the level of inflammatory cytokines . However, TSST-1 protein was unable to induce traditional activation and apoptosis on human platelets . These results suggested that TSST-1 protein may exert indirect effects on platelet activation and apoptosis .
血小板减少症或血小板功能障碍是严重感染的危险因素。金黄色葡萄球菌释放多种毒力因子,特别是中毒性休克综合征毒素 1(TSST-1),可能引起中毒性休克综合征。当携带 基因时,更容易引起中毒性休克综合征,并且死亡率特别高。然而,TSST-1 蛋白对血小板的作用尚不清楚。携带 基因阳性菌血症的患者表现出更严重的感染、更高的死亡率和更低的血小板计数。基因阳性株除了激活 Caspase-3 外,还诱导更多的血小板凋亡和活化以及相应的 Bak 上调和 Bcl-XL 下调。感染基因阳性株的 C57BL/6 小鼠导致血小板计数减少、血小板凋亡和/或活化事件增加以及死亡率增加。此外,由 基因编码的 TSST-1 蛋白导致血小板计数减少、血小板凋亡和活化事件增加以及炎症细胞因子水平升高。然而,TSST-1 蛋白不能诱导人血小板的传统活化和凋亡。这些结果表明,TSST-1 蛋白可能对血小板的活化和凋亡产生间接影响。